In congestive heart failure, patients appear to have a limited ability to dilate their resistance vessels in skeletal muscle in response to a metabolic stimulus. This is true whether the metabolic stimulus is ischemia, dynamic, or static exercise. The mechanism for this limited arteriolar capacity is at least twofold; an increased sodium content of the vessels as well as an increased tissue pressure which is seen in edematous states. This can be considered a positive compensatory mechanism in that it helps to maintain systemic arterial pressure during exercise when the cardiac output fails to increase normally. If the resistance vessels were to dilate normally, then in the face of a limited cardiac output, exercise syncope would be expected to occur. Such a situation does, in fact, occur when patients with congestive heart failure are subjected to intense diuresis. The price paid by heart failure patients for the maintenance of arterial pressure during exercise is an earlier shift to anaerobic metabolism. Because of the limited blood flow to exercising muscle, there is an increased oxygen extraction as the blood traverses the metabolically active muscular beds. This increased oxygen extraction, however, is not sufficient to allow aerobic metabolism to proceed normally. Hence, patients with heart failure are more subject to developing metabolic acidosis during exercise and at lesser levels of exertion than their normal counterparts. This may partly explain the greater oxygen debt seen in patients with congestive heart failure following exercise. A second abnormality present in the peripheral circulations of patients with congestive heart failure is an increased sympathetic alpha adrenergic tone as well as an increased level of circulating catecholamines. This is most true in symptomatic patients at rest and during exertion in most patients with heart failure who are limited in their exercise capacity. This increased sympathetic tone helps to explain the seemingly paradoxical cardiovascular response to certain maneuvers such as head up-tilting and to certain drugs such as digitalis. During exercise, the sympathetic nervous system appears to be activated to a greater extent in patients with congestive heart failure and, as expected, the circulations with the greatest population of alpha receptors, the cutaneous, renal, and splanchnic circulations, appear to suffer the most from an inadequate blood flow. The failure to dilate the cutaneous circulation in response to a thermal stress makes these patients particularly susceptible to cardiac failure in a hot and humid environment. The failure to handle even the normal thermogenesis of mild exertion helps to explain the slight temperature elevations so commonly seen when patients are hospitalized with acute cardiac failure. The failure to cool muscles appropriately during exercise might even contribute to a greater alactic portion of the oxygen debt, as well.69. In the capacitance vessels of the limbs of heart failure patients, there is an increased venous tone, as well. This is minimally related to increased sympathetic efferent impulses to the cutaneous veins and increased circulating catecholamines but is majorly explained on the basis of local factors that go into determining venous tone. The most important local factor that can reduce the venous volume is edema. Since the venous volume of the limbs if reduced only slightly by the increased sympathetic tone in congestive heart failure, it might be expected that drugs such as morphine which seem to work by producing a central nervous system "sympatholysis" would be expected to increase the venous volume of the limbs only minimally. Thus, in acute pulmonary edema, if morphine induces a peripheral pooling of blood, it is likely that it is through its arteriolar dilator mechanism and the perfusion of previously unperfused vascular beds, leading to a passive filling of the venous system.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine